Abstract

There is no generally accepted scientific theory for the cause of adolescent idiopathic
scoliosis (AIS). As part of its mission to widen understanding of scoliosis etiology,
the International Federated Body on Scoliosis Etiology (IBSE).introduced the electronic
focus group (EFG) as a means of increasing debate on knowledge of important topics.
This has been designated as an on-line Delphi discussion. The text for this debate
was written by Dr TB Grivas. It is based on published research from Athens, Greece
evaluating schoolchildren age 11–17 years for the relation of body mass index (BMI)
to each of truncal asymmetry (TA) and menarcheal status. Girls with relatively lower
BMI were found to have a significant excess of severe TAs and significantly later
menarche confirming the well-known relation of BMI to menarche. Together with other
evidence linking nutritional status to skeletal growth, the observations suggest energy
balance via the hypothalamus is related to trunk asymmetry. As with a recent speculative
hypothesis for the pathogenesis of AIS in girls, Grivas et al. suggest that the severe
TAs involve a genetically-determined selectively increased sensitivity (up-regulation)
of the hypothalamus to circulating leptin with asymmetry as an adverse response to
stress (hormesis). The TA is expressed bilaterally via the sympathetic nervous system
to produce left-right asymmetry in ribs and/or vertebrae leading to severe TAs when
beyond the capacity of postural mechanisms of the somatic nervous system to control
the shape distortion in the trunk. This EFG discusses the findings and interpretations
of the paper by Grivas and colleagues as research at the borderland between the genesis
of TA (physiogenesis) and AIS (pathogenesis). It is suggested that TAs, here regarded
in common with AIS, result from the combination of secondary sexual development affecting
body composition, adolescent skeletal growth velocity, and an asymmetry process. The
possible involvement of epigenetic factors is not considered.